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SP15 Pathology > Exam 1; Cell Injury, Cell Death, and Cell Adaptations > Flashcards

Exam 1; Cell Injury, Cell Death, and Cell Adaptations Flashcards

1
Q

This describes the origin of disease, including underlying cause and modifiers; WHY a disease occurs

A

etiology

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2
Q

This describes the development of disease, from molecular/cellular changes to functional and structural abnormalities; HOW a disease occurs

A

pathogenesis

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3
Q

True or False
Clinical signs and symptoms of disease are usually simultaneously associated with the biochemical changes associated with cell injury

A

False; the clinical signs and symptoms are usually several steps removed

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4
Q

What four things can cause decreased O2 (hypoxia) or no O2 (anoxia)

A

impaired absorption of oxygen
decreased blood flow (ischemia)
disease of blood or blood vessels
inadequate oxygenation of the blood

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5
Q

Decreased oxygen impairs this in the mitochondria

A

oxidative phosphorylation; which reduces the amount of ATP which reduces the ability of the plasma membrane to maintain homeostasis

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6
Q

Decrease oxygen causes a net gain of what in the mitochondria

A

a net gain of solute and an isosmotic gain in cytoplasmic water; affects of the ion pumps

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7
Q

When the mitochondria have an isosmotic gain in cytoplasmic water, what three things occur

A
  1. cell swelling with the formation of cell surface blebs
  2. swelling of mitochondria
  3. dilation of the endoplasmic reticulum that leads to detachment of ribosomes from the RER and dissociation of polysomes and decrease in protein synthesis; increasing lipid deposition
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8
Q

Reduced oxidative phosphorylation in the mito leads to an increase in what

A

glycolysis

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9
Q

What happens to the mito where there is an increase in glycolysis

A

increased production of lactic acid and inorganic phosphates which decreases pH and leads to chromatin clumping

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10
Q

This describes a reduced substrate for ATP production which can result in the same patterns as hypoxia/anoxia

A

hypoglycemia

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11
Q

The generation of ROS can be associated with what 5 different processes

A 
inflammation
oxygen toxicity
chemicals
irradiation
aging
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12
Q

This type of ROS is inactivated spontaneously or by superoxide disputes (SOD) to form H2O2

A

superoxide

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13
Q

This type of ROS is detoxified by glutathione peroxidase and catalase

A

hydrogen peroxide

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14
Q

This type of ROS are generated by hydrolysis of water by ionizing radiation or by transitional metals such as Fe++ or Cu++

A

hydroxyl radicals

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15
Q

In which three ways do ROS damage cells

A

lipid peroxidation
protein cross-linking
reacts with thymidine and guanine to induce single strand DNA breaks

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16
Q

These systems in the body act to reduce the effects of ROS by blocking their initiation or by inactivating them

A

intracellular and extracellular antioxidant systems

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17
Q

What are some examples of the intracellular antioxidant system

A

SOD
catalase
glutathione peroxidase

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18
Q

What are some examples of the extracellular antioxidant system

A

vitamins E, A, C

serum proteins that bind free iron and copper

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19
Q

ROS cause what type of damage to DNA

A

single stranded breaks

typically seen in thymidine and guanine

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20
Q

How is the proper level of cytoplasmic Ca maintained

A

by protein sequestration in the cytoplasm, mito, and ER

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21
Q

High levels of Ca will activate which four degradative enzymes

A

ATPase
phospholipases
endonucleases
proteases

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22
Q

What are some additional ways a cell membrane can be injured

A 
complement
cytotoxic T cells
virus
bacterial endotoxins and exotoxins
drugs
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23
Q

True or False

biochemical alterations occur prior to morphologic changes

A

True

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24
Q

The degree of cell injury is determined by what

A

physiologic state of the cell
cell type
intensity, duration and/or number of exposures to the etiological agent

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25
Q

Cell injury may result in what four things

A

reversible cell injury
cellular adaptations associated with changes in cell number, size, or differentiation
cellular adaptations associated with abnormal accumulations
cell death - necrosis or apoptosis

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26
Q

This is acute in nature and occurs when the cell cannot maintain normal homeostasis due to cell injury of short duration and minimal intensity

A

reversible cell injury

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27
Q

What are four common etiologies of a reversible cell injury

A

toxins
infectious agents
hypoxia
thermal injury

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28
Q

What are the two morphologic changes of a cell during reversible cell injury

A

plasma membrane injury leads to an increased intracellular Na that leads to an isosmotic gain in water - edema
organelles and cells swill, and the organ may appear pale and swollen

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29
Q

True or False

There is no signature biochemical event that equates with cell death

A

True

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30
Q

What five morphologic changes take place during necrosis

A

cell swelling
protein denaturation yielding a glassy homogeneous cytoplasm
organelle breakdown may result in vacuolated cytoplasm
nuclei changes
inflammation

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31
Q

The type of necrosis is dependent upon what

A

patterns of enzymatic degradation and by bacterial products when present

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32
Q

This is the most common form of necrosis

A

coagulative; cytoplasmic proteins are coagulated

33
Q

What are the characteristics of coagulative necrosis

A

the nucleus is lost, but the eosinophilic outline of the cell is retained for a short time prior to being removed by the inflammatory response
- cell outline, pink cytoplasm, anucleated cells

34
Q

This type of necrosis is when the tissue is totally digested by the release of lysosomal enzymes during the acute inflammatory response; often associated with focal bacterial or fungal infections, also seen in the CNS

A

liquefactive necrosis (pus)

35
Q

This type of necrosis is associated with M. tuberculosis infection; the tissue has a white and “cheesy” appearance on gross examination

A

caseous necrosis

36
Q

This type of necrosis is common in trauma to the breast or in cases of pancreatitis; adipose tissue has a chalky white-yellow appearance. “soap bubble” histologic appearance

A

fat necrosis

37
Q

What are the morphologic features of apoptosis

A

cell shrinkage
chromatin condensation followed by fragmentation
apoptotic bodies formation
phagocytosis of the apoptotic bodies without a significant inflammatory response

38
Q

What types of disorders can be caused by excess apoptosis

A 
AIDS
ischemia
neurodegenerative diseases
myelodysplasia
toxin induced liver injury
39
Q

What types of disorders can be caused by inhibition of apoptosis

A

cancer
autoimmune diseases
viral diseases

40
Q

What is the mechanism of action of apoptosis

A

signaling
control and integration
execution
removal of dead cells

41
Q

What are the signaling methods involving apoptosis

A

direct signaling

regulation of mitrochondrial permeability

42
Q

These genes serve as an on/off switch that regulates the permeability of the mito during apoptosis

A

Bcl-2 gene family

43
Q

These Bcl genes inhibit apoptosis

A

Bcl-2

Bcl-x

44
Q

These Bcl genes stimulate apoptosis

A

Bax

bak

45
Q

This is released from the outer mitochondria membrane and serves to disrupt the inhibitory function of Bcl-2 therefore FAVORING apoptosis

A

cytochorome c

46
Q

Apoptosis signaling pathways converge on an autocatalytic proteolytic cascade of what, which can “execute” the cell

A

caspases

47
Q

The mitochondria release this, that activated various enzymes like transglutaminases and endonucleases

A

Ca

48
Q

In which ways are the dead cells removed

A

phagocytosis of deal cells and macrophages

there is little/no inflammation

49
Q

How do apoptosis and necrosis differ in regards to stimuli

A

apoptosis - physiologic and pathologic

necrosis - hypoxia and toxins

50
Q

How do apoptosis and necrosis differ in regards to morphology

A

Apoptosis - single cell, shrinkage, condensed chromatic, intact plasma membrane, apoptotic bodies
necrosis - multiple cells, swelling, lysed plasma membrane, organelle disruption

51
Q

How do apoptosis and necrosis differ in regards to the mechanism of DNA destruction

A

apoptosos - ATP dependent process, gene activation and endonuclease mediated DNA fragmentation
necrosis - ATP independent process, random, diffuse, ROS, membrane injury

52
Q

How do apoptosis and necrosis differ in regards to tissue reaction

A

apoptosis - minimal inflammation, phagocytosis of apoptotic bodies
necrosis - inflammation

53
Q

cells undergo this type of change due to persistent (chronic) stresses

A

adaptative changes

54
Q

True or False

morphologic changes seldom specific to the type of persistent stress

A

True

55
Q

This is a decrease in cell size and function with concurrent decrease in organ size and/or function

A

atrophy

56
Q

What are some etiologies of atrophy

A 
decreased workload
loss of innervation
decreased blood supply
inadequate nutrition
decreased hormonal stimulation
aging
local pressure
57
Q

This is an increase in cell size and function with concurrent increase in organ size and/or function

A

hypertrophy

58
Q

What are the etiologies of hypertrophy

A

increased functional demand
increased or imbalanced nutrition
increased hormonal stimulation

59
Q

This is an increase in cell number with concurrent increase in organ size and/or function

A

hyperplasia

60
Q

What are the etiologies of hyperplasia

A

hormones and growth factors

wound healing

61
Q

This is the alteration in cell differentiation with concurrent alteration of tissue/organ function
one adult cell type is replaced by another adult cell type in response to chronic stress

A

metaplasia

62
Q

What are the etiologies of metaplasia

A

intestional; replacement of normal epithelium to intentional mucus-type cells
squamous; normal columnar epithelium to stratified squamous (smokers)

63
Q

What are the categories of cell accumulations

A

excess of normal cellular constituent such as H20, lipids, proteins, and carbohydrates, and pigments that may be endogenous or exogenous

64
Q

What are the four mechanisms of intracellular accumulations

A

abnormal metabolism
lack of an enzyme
abnormal protein folding or transport
ingestion of indigestible material

65
Q

What can occur with lipid accumulation

A

steatosis (fatty liver); abnormal accumulation of triglycerides within the parenchymal cells of the liver, heart, kidney, and muscles

66
Q

What can be the etiology of steatosis

A 
obesity
diabetes
EtOH
anorexia
toxins
protein malnutrition
67
Q

What is the gross appearance of steatosis

A

enlarged yellow (liver)

68
Q

What is the microscopic appearance of steatosis

A

hepatocytes contain clear cytoplasmic vacuoles that displace the nucleus

69
Q

This accumulates primarily in macrophages; in the sub epithelial macrophages forming xanthoma and in the vessels forming atheromas

A

cholesterol

70
Q

What is the histology of protein accumulation

A

eosinophilic cytoplasmic droplets, vacuoles, or aggregates

71
Q

What are some examples of disorders of protein accumulation

A 
ɑ-1-anti-trypsin deficiency
mallory bodies (improper folding)
neurofibrillary tangles in Alzheimers
72
Q

What is the morphology of excess glycogen/glucose

A

clear, cytoplasmic/nuclear vacuoles

73
Q

What are some examples of exogenous pigmentation

A

carbon accumulated in macrophages, anthracosis vs. pneumoconiosis
tattoos

74
Q

What are some examples of endogenous pigmentation

A

lipofuscin
melanin
hemosiderin
bilirudin

75
Q

This is an endogenous pigment that is “wear and tear” “brown-yellow granular pigment
a lipoprotein complex due to ROS preoxidation of membranes

A

lipofuscin

76
Q

This is an endogenous pigment that is black-brown, produced by melanocytes but accumulated in adjacent epidermal cells and in macrophages

A

melanin

77
Q

This is an endogenous pigment that is yellow-brown representing aggregates of ferritin micelles; accumulation from excess iron locally due to hemorrhage.

A

hemosiderin

78
Q

This is a genetic disease associated with cell death due to uncompensated hemosiderin accumulation

A

hemochromatosis

79
Q

This is an endogenous pigment that is yellow-brown and is the end product of heme metabolism; it accumulates in hepatocytes and bile ducts due to hemolysis, obstructed bile flow, and/or hepatocellular disease

A

bilirudin

SP15 Pathology (17 decks)

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